Vy H Nguyen, Audrey Ha, Nicholas Ajit Rouillard, Richard Hieu Le, Ashley Fong, Surya Gudapati, Jung Eun Park, Mayumi Maeda, Scott Barnett, Ramsey Cheung, Mindie H Nguyen
{"title":"Differential Mortality Outcomes in Real-world Patients with Lean, Nonobese, and Obese Nonalcoholic Fatty Liver Disease.","authors":"Vy H Nguyen, Audrey Ha, Nicholas Ajit Rouillard, Richard Hieu Le, Ashley Fong, Surya Gudapati, Jung Eun Park, Mayumi Maeda, Scott Barnett, Ramsey Cheung, Mindie H Nguyen","doi":"10.14218/JCTH.2023.00016","DOIUrl":"10.14218/JCTH.2023.00016","url":null,"abstract":"<p><strong>Background and aims: </strong>Nonalcoholic fatty liver disease (NAFLD) is commonly associated with obesity but can develop in normal-weight people (lean NAFLD). We compared outcomes in lean, overweight, and obese NAFLD.</p><p><strong>Methods: </strong>This retrospective chart review included patients at Stanford University Medical Center with NAFLD confirmed by imaging between March 1995 and December 2021. Lean, overweight, and obese patients had body mass index of <25.0, >25.0 and <29.9, and ≥30.0 kg/m<sup>2</sup> for non-Asian and >23.0 and ≥27.5 for overweight and obese Asian patients.</p><p><strong>Results: </strong>A total of 9061 lean (10.2%), overweight (31.7%), and obese (58.1%) patients were included. Lean patients were 5 years older than obese patients (53±17.4 vs. 48.7±15.1 years), more were female (59.6% vs. 55.2%), white (49.1% vs. 46.5%), had NASH (29.2% vs. 22.5%), cirrhosis (25.3% vs.19.2%), or nonliver cancer (25.3% vs. 18.3%). Fewer had diabetes (21.7% vs. 35.8%) or metabolic comorbidities (all <i>p</i><0.0001). Lean NAFLD patients had liver-related mortality similar to other groups but higher overall (<i>p</i>=0.01) and nonliver-related (<i>p</i>=0.02) mortality. After multivariable model adjustment for covariates, differences between lean and obese NAFLD in liver-related, nonliver-related, and overall mortality (adjusted hazard ratios of 1.34, 1.00, and 1.32; <i>p</i>=0.66, 0.99, and 0.20, respectively) were not significant.</p><p><strong>Conclusions: </strong>Lean NAFLD had fewer metabolic comorbidities but similar adverse or worse outcomes, suggesting that it is not benign. Healthcare providers should provide the same level of care and intervention as for overweight and obese NAFLD.</p>","PeriodicalId":15484,"journal":{"name":"Journal of Clinical and Translational Hepatology","volume":"11 7","pages":"1448-1454"},"PeriodicalIF":3.6,"publicationDate":"2023-12-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10752812/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139074255","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Focal Nodular Hyperplasia: A Comprehensive Review with a Particular Focus on Pathogenesis and Complications","authors":"Jaimy Villavicencio Kim, George Y. Wu","doi":"10.14218/jcth.2023.00265","DOIUrl":"https://doi.org/10.14218/jcth.2023.00265","url":null,"abstract":"","PeriodicalId":15484,"journal":{"name":"Journal of Clinical and Translational Hepatology","volume":"26 23","pages":""},"PeriodicalIF":3.6,"publicationDate":"2023-12-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138950421","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Journal of Clinical and Translational Hepatology 10th Anniversary Editorial","authors":"","doi":"10.14218/jcth.2023.00001","DOIUrl":"https://doi.org/10.14218/jcth.2023.00001","url":null,"abstract":"","PeriodicalId":15484,"journal":{"name":"Journal of Clinical and Translational Hepatology","volume":"124 7","pages":""},"PeriodicalIF":3.6,"publicationDate":"2023-12-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138958965","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Predictive Model of Oxaliplatin-induced Liver Injury Based on Artificial Neural Network and Logistic Regression","authors":"Rui Huang, Yuanxuan Cai, Yisheng He, Zao-qin Yu, Li Zhao, Tao Wang, Xiaofang Shangguan, Yuhang Zhao, Zherui Chen, Yunzhou Chen, Chengliang Zhang","doi":"10.14218/jcth.2023.00399","DOIUrl":"https://doi.org/10.14218/jcth.2023.00399","url":null,"abstract":"","PeriodicalId":15484,"journal":{"name":"Journal of Clinical and Translational Hepatology","volume":"1 6","pages":""},"PeriodicalIF":3.6,"publicationDate":"2023-12-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138601315","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Liver Lesions at Risk of Transformation into Hepatocellular Carcinoma in Cirrhotic Patients: Hepatobiliary Phase Hypointense Nodules without Arterial Phase Hyperenhancement","authors":"N. Brandi, Matteo Renzulli","doi":"10.14218/jcth.2023.00130","DOIUrl":"https://doi.org/10.14218/jcth.2023.00130","url":null,"abstract":"","PeriodicalId":15484,"journal":{"name":"Journal of Clinical and Translational Hepatology","volume":"12 1","pages":""},"PeriodicalIF":3.6,"publicationDate":"2023-11-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139211484","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Yining Zou, Kun Zhu, Yanrui Pang, Jing Han, Xin Zhang, Zhengzeng Jiang, Yufeng Huang, Wenyi Gu, Yuan Ji
{"title":"Molecular Detection of <i>FGFR2</i> Rearrangements in Resected Intrahepatic Cholangiocarcinomas: FISH Could Be An Ideal Method in Patients with Histological Small Duct Subtype.","authors":"Yining Zou, Kun Zhu, Yanrui Pang, Jing Han, Xin Zhang, Zhengzeng Jiang, Yufeng Huang, Wenyi Gu, Yuan Ji","doi":"10.14218/JCTH.2022.00060S","DOIUrl":"10.14218/JCTH.2022.00060S","url":null,"abstract":"<p><strong>Background and aims: </strong>Intrahepatic cholangiocarcinoma (ICC) is a subtype of primary liver cancer for which effective therapeutic agents are lacking. Fibroblast growth factor receptor 2 (<i>FGFR2</i>) has become a promising therapeutic target in ICC; however, its incidence and optimum testing method have not been fully assessed. This study investigated the rearrangement of <i>FGFR2</i> in intrahepatic cholangiocarcinoma using multiple molecular detection methods.</p><p><strong>Methods: </strong>The samples and clinical data of 167 patients who underwent surgical resection of intrahepatic cholangiocarcinoma in Zhongshan hospital, Fudan university were collected. The presence of <i>FGFR2</i> gene rearrangement was confirmed using fluorescence in situ hybridization (FISH) and targeted next-generation sequencing (NGS). <i>FGFR2</i> protein expression was determined using immunohistochemistry (IHC). The concordance between the methods was statistically compared. PD-L1 expression was also assessed in this cohort. The clinicopathological characteristics and genomic profile related to <i>FGFR2</i> rearrangements were also analyzed to assist candidate-screening for targeted therapies.</p><p><strong>Results: </strong><i>FGFR2</i> rearrangement was detected in 21 of the 167 ICC cases (12.5%) using FISH. NGS analysis revealed that <i>FGFR2</i> rearrangement was present in 16 of the 20 FISH-positive cases, which was consistent with the FISH results (kappa value=0.696, <i>p</i><0.01). IHC showed that 80 of the 167 cases (48%) were positive for <i>FGFR2</i> expression, which was discordant with both FISH and NGS results. By comparison, <i>FGFR2</i>-positivity tended to correlate with unique clinicopathological subgroups, featuring early clinical stage, histologically small duct subtype, and reduced mucus production (P<0.05), with improved overall survival (<i>p</i><0.05). <i>FGFR2</i>-positivity was not associated with PD-L1 expression in ICCs. In genome research, we identified eight partner genes fused with <i>FGFR2</i>, among which <i>FGFR2-BICC1</i> was the most common fusion type. <i>BAP1, CDKN2A,</i> and <i>CDKN2B</i> were the most common concomitant genetic alterations of <i>FGFR2</i>, whereas <i>KRAS</i> and <i>IDH1</i> mutations were mutually exclusive to <i>FGFR2</i> rearrangements.</p><p><strong>Conclusions: </strong>FISH achieved satisfactory concordance with NGS, has potential value for <i>FGFR2</i> screening for targeted therapies. <i>FGFR2</i> detection should be prioritized for unique clinical subgroups in ICC, which features a histological small duct subtype, early clinical stage, and reduced mucus production.</p>","PeriodicalId":15484,"journal":{"name":"Journal of Clinical and Translational Hepatology","volume":"11 6","pages":"1355-1367"},"PeriodicalIF":3.1,"publicationDate":"2023-11-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/43/28/JCTH-11-1355.PMC10500298.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10299947","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Fucoidan Ameliorates Ferroptosis in Ischemia-reperfusion-induced Liver Injury through Nrf2/HO-1/GPX4 Activation.","authors":"Jing-Jing Li, Wei-Qi Dai, Wen-Hui Mo, Wen-Qiang Xu, Yue-Yue Li, Chuan-Yong Guo, Xuan-Fu Xu","doi":"10.14218/JCTH.2023.00133","DOIUrl":"10.14218/JCTH.2023.00133","url":null,"abstract":"<p><strong>Background and aims: </strong>Liver ischemia-reperfusion (IR) injury is a common pathological process in liver surgery. Ferroptosis, which is closely related to lipid peroxidation, has recently been confirmed to be involved in the pathogenesis of IR injury. However, the development of drugs that regulate ferroptosis has been slow, and a complete understanding of the mechanisms underlying ferroptosis has not yet been achieved. Fucoidan (Fu) is a sulfated polysaccharide that has attracted research interest due to its advantages of easy access and wide biological activity.</p><p><strong>Methods: </strong>In this study, we established models of IR injury using erastin as an activator of ferroptosis, with the ferroptosis inhibitor ferrostatin-1 (Fer-1) as the control. We clarified the molecular mechanism of fucoidan in IR-induced ferroptosis by determining lipid peroxidation levels, mitochondrial morphology, and key pathways in theta were involved.</p><p><strong>Results: </strong>Ferroptosis was closely related to IR-induced hepatocyte injury. The use of fucoidan or Fer-1 inhibited ferroptosis by eliminating reactive oxygen species and inhibiting lipid peroxidation and iron accumulation, while those effects were reversed after treatment with erastin. Iron accumulation, mitochondrial membrane rupture, and active oxygen generation related to ferroptosis also inhibited the entry of nuclear factor erythroid 2-related factor 2 (Nrf2) into the nucleus and reduced downstream heme oxygenase-1 (HO-1) and glutathione peroxidase 4 (GPX4) protein levels. However, fucoidan pretreatment produced adaptive changes that reduced irreversible cell damage induced by IR or erastin.</p><p><strong>Conclusions: </strong>Fucoidan inhibited ferroptosis in liver IR injury via the Nrf2/HO-1/GPX4 axis.</p>","PeriodicalId":15484,"journal":{"name":"Journal of Clinical and Translational Hepatology","volume":"11 6","pages":"1341-1354"},"PeriodicalIF":3.1,"publicationDate":"2023-11-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/5c/32/JCTH-11-1341.PMC10500289.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10299948","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Guidelines for the Prevention and Treatment of Chronic Hepatitis B (version 2022).","authors":"Hong You, Fusheng Wang, Taisheng Li, Xiaoyuan Xu, Yameng Sun, Yuemin Nan, Guiqiang Wang, Jinlin Hou, Zhongping Duan, Lai Wei, Jidong Jia, Hui Zhuang","doi":"10.14218/JCTH.2023.00320","DOIUrl":"10.14218/JCTH.2023.00320","url":null,"abstract":"<p><p>To facilitate the achieving of the goal of \"eliminating viral hepatitis as a major public health threat by 2030\" set by the World Health Organization, the Chinese Society of Hepatology together with the Chinese Society of Infectious Diseases (both are branches of the Chinese Medical Association) organized a panel of experts and updated the guidelines for prevention and treatment of chronic hepatitis B in China (version 2022). With the support of available evidence, this revision of the guidelines focuses on active prevention, large scale testing, and expansion of therapeutic indication of chronic hepatitis B with the aim of reducing the hepatitis B related disease burden.</p>","PeriodicalId":15484,"journal":{"name":"Journal of Clinical and Translational Hepatology","volume":"11 6","pages":"1425-1442"},"PeriodicalIF":3.1,"publicationDate":"2023-11-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/24/78/JCTH-11-1425.PMC10500285.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10308008","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Bin Fan, He Xie, Qi Tan, Qingyuan Li, Tao Gong, Baoren He, Yujia Li, Limin Chen
{"title":"Role of Exosomal Modulation of Macrophages in Liver Fibrosis","authors":"Bin Fan, He Xie, Qi Tan, Qingyuan Li, Tao Gong, Baoren He, Yujia Li, Limin Chen","doi":"10.14218/jcth.2023.00381","DOIUrl":"https://doi.org/10.14218/jcth.2023.00381","url":null,"abstract":"","PeriodicalId":15484,"journal":{"name":"Journal of Clinical and Translational Hepatology","volume":"196 ","pages":""},"PeriodicalIF":3.6,"publicationDate":"2023-11-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139245494","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}